Synopsis
Recognise haematological and neurological vitamin B12 deficiency, determine whether autoimmune gastritis or another cause is responsible, and replace promptly with route and duration matched to reversibility.
- Vitamin B12 deficiency can present with neuropathy, impaired vibration or joint position, ataxia, cognitive or psychiatric change, glossitis or fatigue before anaemia or macrocytosis appears.
- Take pretreatment blood when this causes no harmful delay. Interpret total or active B12 through NICE NG239 thresholds and use methylmalonic acid or homocysteine when the result is indeterminate and symptoms persist.
- Nitrous oxide can produce functional deficiency despite a non-low serum B12. NICE recommends homocysteine or methylmalonic acid testing, but neurological treatment must not wait when suspicion is strong.
Key red flags
Symmetrical paraesthesia, impaired vibration or proprioception, sensory ataxia, weakness, cognitive change or visual symptoms with risk factors warrants prompt assessment and replacement.
Investigation priorities
Classify the initial result within the NICE diagnostic pathway.
Management branches
Neurological symptoms and risk factors suggest vitamin B12 deficiency or nitrous-oxide-mediated functional deficiency.
- Take B12 and functional-marker samples if immediately available, document a full neurological examination and exposure history, and stop nitrous oxide, but do not delay replacement for results.
- Preferred UK treatment is hydroxocobalamin 1 mg intramuscularly on alternate days until no further improvement, followed by the maintenance schedule when the cause is irreversible.
Key medicines
Hydroxocobalamin with neurological involvementGive 1 mg intramuscularly on alternate days until no further improvement, then 1 mg every 2 months when the underlying cause is irreversible.
Hydroxocobalamin without neurological involvementGive 1 mg intramuscularly three times a week for 2 weeks, then 1 mg every 2 to 3 months when ongoing maintenance is required.